Going on and on with NO?
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Administration, Inhalation↗
Biomedical subjects
Paul Steendijk
Publications and source records attributed to Paul Steendijk.
Does a gender difference in response to cardiac resynchronization therapy exist?
BACKGROUND: Cardiac resynchronization therapy (CRT) has a beneficial effect on clinical symptoms, exercise capacity, and systolic left ventricular (LV) performance in patients with heart failure. The aim of the current study was to evaluate whether a gender difference exists in response to CRT. METHODS: Consecutive patients with end-stage heart failure (New York Heart Association, NYHA, class III-IV), LV ejection fraction (LVEF) < or =35%, QRS duration >120 ms, and left bundle branch block configuration underwent CRT. At baseline and 6 months post-CRT, clinical and echocardiographic parameters were evaluated; follow-up was obtained up to 5 years. The effects of CRT were compared between women and men. RESULTS: The study population comprised 137 men and 36 women (mean age 66 +/- 11 years). No differences in baseline characteristics were observed except that nonischemic cardiomyopathy was more frequent in women than men (67% vs 38%, P < 0.05). In all patients, clinical and echocardiographic parameters improved significantly at 6-month follow-up. The magnitude of improvement in different parameters was similar between women and men, e.g., the improvement in NYHA Class was 0.9 +/- 0.6 in women and 1.0 +/- 0.7 in men (NS) and the increase in LVEF was 8 +/- 8% in women as compared to 7 +/- 9% in men (NS). The percentage of individual responders was not different between women and men (76% vs 80%, NS) and 2-year survival was comparable for women and men (84% vs 80%, NS). CONCLUSION: No gender differences were observed in response to CRT and long-term survival after CRT.
Cardiac Pacing, Artificial↗
Long-term follow-up of cardiac resynchronization therapy in patients with end-stage heart failure.
UNLABELLED: Long-term follow-up of cardiac resynchronization therapy. INTRODUCTION: Cardiac resynchronization therapy (CRT) has been introduced to treat patients with end-stage heart failure, and results of this technique are promising. The aim of our study was to assess the sustained benefit of CRT in a large patient cohort with end-stage heart failure at long-term follow-up. In addition, the prognosis of responders and nonresponders was evaluated. METHODS AND RESULTS: 125 patients with end-stage heart failure, NYHA class III or IV, LVEF<35%, QRS duration>120 msec and left bundle branch block morphology received a biventricular device. At baseline and 6 months after implantation the following parameters were evaluated: NYHA class, Minnesota Quality of life score, QRS duration on surface ECG, 6-minute walking distance and LVEF. Follow-up was obtained up to 3 years. After 6 months, patients were divided in clinical responders and nonresponders according to improvement in NYHA class. All clinical parameters improved significantly at 6-month follow-up. Hospitalization for heart failure was 3.8+/-4.9 days/year before and 0.7+/-1.6 days/year after CRT. Survival at 1-, 2-, and 3-year follow-up was 93%, 88%, and 85%, respectively. Responders (78%) showed a significantly better survival than nonresponders at 2- and 3-year follow-up (96% and 93% for responders versus 81% and 73% for nonresponders, P<0.05). CONCLUSION: The improvement in functional status and symptoms after CRT is maintained at long-term follow-up (up to 3 years). The clinical improvement was associated with a significant reduction in hospitalization rate which was also maintained over the years. Preimplantation selection of responders may result in even better long-term survival.
Aged↗
Angiotensin AT2 receptor deficiency after myocardial infarction: its effects on cardiac function and fibrosis depend on the stimulus.
Hearts of normotensive angiotensin II type 2 receptor (AT2)-deficient mice do not develop fibrosis after angiotensin II-induced chronic hypertension. Thus, the goal of our study was to clarify whether AT2 knockouts (KOs) are also characterized by altered left ventricular (LV) function and modified remodeling of the extracellular matrix (ECM) after induction of myocardial infarction (MI). MI was induced in 5-mo-old female AT2-deficient mice and controls by occlusion of the left coronary artery. Time-matched sham-operated animals served as controls. After 48 h, the first sets of mice were hemodynamically characterized using a pressure-tip catheter (n = 8/group). We also obtained pressure volume loops using a microconductance catheter in additional sets of animals 3 wk after induction of MI (n = 7/group). Finally, the collagen index was illustrated by Sirius red staining and quantified by digital analysis. Whereas the LV function of sham-operated animals did not differ between both genotypes, the collagen index was 44% lower in KO animals. Forty-eight hours and 3 wk post-MI, systolic and diastolic LV function were impaired in both AT2-deficient and wild-type (WT) animals to the same extent by approx 45%. No differences were found between the two genotypes with respect to LV hypertrophy and the fibrosis index in the infarcted and noninfarcted areas 3 wk post-MI. While AT2-KO mice had less cardiac collagen content under basal conditions, the receptor deficiency had no significant influence on LV function at the two investigated time points after induction of MI or on the remodeling of ECM at the latter time point. Thus, hypertension-induced fibrosis is probably triggered by other control mechanisms than fibrosis induced by MI.
Animals↗
Comparison of response to cardiac resynchronization therapy in patients with sinus rhythm versus chronic atrial fibrillation.
Cardiac resynchronization therapy (CRT) is a new therapeutic option for patients who have drug-refractory end-stage heart failure. Much information has been obtained from patients who have sinus rhythm, but the use of CRT in patients who have chronic atrial fibrillation (AF) has not been studied extensively. Accordingly, we evaluated the clinical response and long-term survival rate of CRT in patients who had heart failure and chronic AF, and the results were compared with those in patients who had sinus rhythm and who underwent CRT. Sixty patients who had end-stage heart failure (30 had sinus rhythm and 30 had chronic AF), New York Heart Association classes III to IV, left ventricular ejection fraction <35%, QRS interval >120 ms, and a left bundle branch block received a biventricular pacemaker. New York Heart Association class, Minnesota Quality of Life score, and 6-minute walking distance were evaluated at baseline and after 6 months of CRT. Long-term follow-up was </=2 years. New York Heart Association class, Minnesota Quality of Life score, and 6-minute walking distance improved significantly in the 2 groups after 6 months of CRT. The number of nonresponders was greater among patients who had AF. Nevertheless, the long-term survival rate was comparable between patients who had sinus rhythm and those who had AF. Patients who had AF demonstrated comparable benefit from CRT as those who had sinus rhythm.
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Reservoir and conduit function of right atrium: impact on right ventricular filling and cardiac output.
The purpose of this study was to investigate the relationship between right atrial (RA) reservoir and conduit function and to determine how hemodynamic changes influence this relationship and its impact on cardiac output. In 11 open-chest sheep, RA reservoir and conduit function were quantified as RA inflow with the tricuspid valve closed versus open, respectively. Conduit function was separated into early (before A wave) and late (after A wave) components. The effects of inotropic stimulation, partial pulmonary artery occlusion, and pericardiotomy were tested. At baseline with the pericardium intact, reservoir function accounted for 0.56 (SD 0.13) of RA inflow, early conduit for 0.29 (SD 0.07), and late conduit (during RA contraction) for 0.16 (SD 0.11). Inotropic stimulation decreased conduit function and increased reservoir function, but these effects did not reach statistical significance. With partial pulmonary artery occlusion, early conduit function fell to 0.20 (SD 0.11) (P < 0.04), and the conduit-to-reservoir ratio decreased by 41% (P < 0.03). Similarly, after pericardiotomy, early conduit function fell to 0.14 (SD 0.09) (P < 0.004), reservoir function increased to 0.72 (SD 0.08) (P < 0.04), and, consequently, the early conduit-to-reservoir ratio decreased by 63% (P < 0.006). Cardiac output was inversely related to the conduit-to-reservoir ratio (r = 0.39, P < 0.001). This study demonstrated that the right atrium adjusts its ability to act more as a reservoir than a conduit in a dynamic manner. The RA conduit-to-reservoir ratio was directly related to the right ventricular pressure-RA pressure gradient at the time of maximum RA volume, with increased ventricular pressures favoring conduit function, but it was inversely related to cardiac output, with an increase in the reservoir contribution favoring improved cardiac output.
Acute Disease↗
Systolic and diastolic ventricular function assessed by pressure-volume loops in the stage 21 venous clipped chick embryo.
Cardiac pressure-volume relations enable quantification of intrinsic ventricular diastolic and systolic properties independent of loading conditions. The use of pressure-volume loop analysis in early stages of development could contribute to a better understanding of the relationship between hemodynamics and cardiac morphogenesis. The venous clip model is an intervention model for the chick embryo in which permanent obstruction of the right lateral vitelline vein temporarily reduces the mechanical load on the embryonic myocardium and induces a spectrum of outflow tract anomalies. We used pressure-volume loop analysis of the embryonic chick heart at stage 21 (3.5 d of incubation) to investigate whether the development of ventricular function is affected by venous clipping at stage 17, compared with normal control embryos. Steady state hemodynamic parameters demonstrated no significant differences between the venous clipped and control embryos. However, analysis of pressure-volume relations showed a significantly lower end-systolic elastance in the clipped embryos (slope of the end-systolic pressure-volume relation: 5.68 +/- 0.85 versus 11.76 +/- 2.70 mm Hg/microL, p < 0.05), indicating reduced contractility. Diastolic stiffness tended to be increased in the clipped embryos (slope of end-diastolic pressure-volume relation: 2.74 +/- 0.56 versus 1.67 +/- 0.21, p = 0.103), but the difference did not reach statistical significance. The results of the pressure-volume loop analysis show that 1 d after venous obstruction, development of ventricular function is affected, with reduced contractility. Pressure-volume analysis may be applied in the chick embryo and is a sensitive technique to detect subtle alterations in ventricular function.
Animals↗
Left ventricular dyssynchrony predicts response and prognosis after cardiac resynchronization therapy.
OBJECTIVES: This study was designed to predict the response and prognosis after cardiac resynchronization therapy (CRT) in patients with end-stage heart failure (HF). BACKGROUND: Cardiac resynchronization therapy improves HF symptoms, exercise capacity, and left ventricular (LV) function. Because not all patients respond, preimplantation identification of responders is needed. In the present study, response to CRT was predicted by the presence of LV dyssynchrony assessed by tissue Doppler imaging. Moreover, the prognostic value of LV dyssynchrony in patients undergoing CRT was assessed. METHODS: Eighty-five patients with end-stage HF, QRS duration >120 ms, and left bundle-branch block were evaluated by tissue Doppler imaging before CRT. At baseline and six months follow-up, New York Heart Association functional class, quality of life and 6-min walking distance, LV volumes, and LV ejection fraction were determined. Events (death, hospitalization for decompensated HF) were obtained during one-year follow-up. RESULTS: Responders (74%) and nonresponders (26%) had comparable baseline characteristics, except for a larger dyssynchrony in responders (87 +/- 49 ms vs. 35 +/- 20 ms, p < 0.01). Receiver-operator characteristic curve analysis demonstrated that an optimal cutoff value of 65 ms for LV dyssynchrony yielded a sensitivity and specificity of 80% to predict clinical improvement and of 92% to predict LV reverse remodeling. Patients with dyssynchrony >/=65 ms had an excellent prognosis (6% event rate) after CRT as compared with a 50% event rate in patients with dyssynchrony <65 ms (p < 0.001). CONCLUSIONS: Patients with LV dyssynchrony >/=65 ms respond to CRT and have an excellent prognosis after CRT.
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Is carbon monoxide-mediated cyclic guanosine monophosphate production responsible for low blood pressure in neonatal respiratory distress syndrome?
Infant respiratory distress syndrome (RDS) involves inflammatory processes, causing an increased expression of inducible heme oxygenase with subsequent production of carbon monoxide (CO). We hypothesized that increased production of CO during RDS might be responsible for increased plasma levels of vasodilatory cGMP and, consequently, low blood pressure observed in infants with RDS. Fifty-two infants (no-RDS, n = 21; RDS, n = 31), consecutively admitted to the neonatal intensive care unit (NICU) between January and October 2003 were included. Hemoglobin-bound carbon monoxide (COHb), plasma cGMP, plasma nitric oxide (NOx), and bilirubin were determined at 0-12, 48-72, and at 168 h postnatally, with simultaneous registration of arterial blood pressure. Infants with RDS had higher levels of cGMP and COHb compared with no-RDS infants (RDS vs. no-RDS: cGMP ranging from 76 to 101 vs. 58 to 82 nmol/l; COHb ranging from 1.2 to 1.4 vs. 0.9 to 1.0%). Highest values were reached at 48-72 h [RDS vs. no-RDS mean (SD): cGMP 100 (39) vs. 82 (25) nmol/l (P < 0.001); COHb 1.38 (0.46) vs. 0.91 (0.26)% (P < 0.0001)]. Arterial blood pressure was lower and more blood pressure support was needed in RDS infants at that point of time [RDS vs. no-RDS mean (SD): mean arterial blood pressure 33 (6) vs. 42 (5) mmHg (P < 0.05)]. NOx was not different between groups and did not vary with time. Multiple linear regression analysis showed a significant correlation between cGMP and COHb, suggesting a causal relationship. Mean arterial blood pressure appeared to be primarily correlated to cGMP levels (P < 0.001). We conclude that a CO-mediated increase in cGMP causes systemic vasodilation with a consequent lower blood pressure and increased need for blood pressure support in preterm infants with RDS.
Biomarkers↗
Heart failure with preserved ejection fraction. Diastolic dysfunction, subtle systolic dysfunction, systolic-ventricular and arterial stiffening, or misdiagnosis?
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Aged↗
Magnetic resonance imaging analysis of right ventricular pressure-volume loops: in vivo validation and clinical application in patients with pulmonary hypertension.
BACKGROUND: The aims of this study were to validate MRI-derived right ventricular (RV) pressure-volume loops for assessment of RV myocardial contractility and then to apply this technique in patients with chronic RV pressure overload for assessment of myocardial contractility, ventricular pump function, and VA coupling. METHODS AND RESULTS: Flow-directed catheters were guided under MR fluoroscopy (1.5 T) into the RV for invasive pressure measurements. Simultaneously, ventricular volumes and myocardial mass were assessed from cine MRI. From sampled data, RV pressure-volume loops were constructed, and maximal ventricular elastance indexed to myocardial mass (E(max_i)) was derived by use of a single-beat estimation method. This MRI method was first validated in vivo (6 swine), with conductance techniques used as reference. Bland-Altman test showed good agreement between methods (E(max_i)=5.1+/-0.5 versus 5.8+/-0.7 mm Hg x mL(-1) x 100 g(-1), respectively; P=0.08). Subsequently, the MRI method was applied in 12 subjects: 6 control subjects and 6 patients with chronic RV pressure overload from pulmonary hypertension. In these patients, indexes of RV pump function (cardiac index), E(max_i), and VA coupling (E(max)/E(a)) were assessed. In patients with pulmonary hypertension, RV pump function was decreased (cardiac index, 2.2+/-0.5 versus 2.9+/-0.4 L x min(-1) x m(-2); P<0.01), myocardial contractility was enhanced (E(max_I), 9.2+/-1.1 versus 5.0+/-0.9 mm Hg x mL(-1) x 100 g(-1); P<0.01), and VA coupling was inefficient (E(max)/E(a), 1.1+/-0.3 versus 1.9+/-0.4; P<0.01) compared with control subjects. CONCLUSIONS: RV myocardial contractility can be determined from MRI-derived pressure-volume loops. Chronic RV pressure overload was associated with reduced RV pump function despite enhanced RV myocardial contractility. The proposed MRI approach is a promising tool to assess RV contractility in the clinical setting.
Adolescent↗
Angiotensin deficiency in mice leads to dilated cardiomyopathy.
To explore the role of angiotensin II, we assessed hemodynamics and cardiac function in angiotensinogen-deficient mice in comparison to wild-type animals. Left ventricular end-diastolic diameter and wall thickness were evaluated by echocardiography and systolic and diastolic left ventricular function by pressure-volume relations using a micro-conductance catheter. Compared to wild-type animals, the angiotensinogen-deficient mice were hypotensive and showed impaired systolic function. The hearts were dilated, demonstrated by echocardiography and by a right-ward shift of the pressure-volume loops, but end-diastolic pressure, isovolumic relaxation (tau) and diastolic stiffness were unchanged. Afterload, however, was reduced leading to maintained cardiac output. Although a blockade of the renin-angiotensin system via angiotensin converting enzyme inhibitors or angiotensin AT1 receptor antagonist is beneficial after cardiac failure, the absence of angiotensin peptides during the ontogenesis leads to dilated cardiomyopathy.
Angiotensin II↗
Transcardiac conductance for continuous measurement of left ventricular volume: validation vs. angiography in patients.
OBJECTIVE: To test the feasibility of the transcardiac conductance (TCC) method for continuous, on-line measurement of absolute left ventricular (LV) volume and to validate the method by comparison with biplane angiography. DESIGN AND SETTING: Prospective clinical feasibility and validation study in a cardiac catheterization laboratory in a university hospital. PATIENTS AND INTERVENTIONS: Ten patients scheduled for electrophysiological studies ( n=5), percutaneous transluminal coronary angioplasty ( n=3), and left- and right-sided cardiac catheterization ( n=2) were enrolled in the feasibility study. Twenty patients scheduled for diagnostic left- and right-sided cardiac catheterization were included in the validation study. The latter were studied at baseline and during right atrial pacing 30 beats/min above baseline. MEASUREMENTS AND RESULTS: In the feasibility study satisfactory ventricular volume signals were obtained by TCC in eight of ten patients. In the validation study calibration factors (alpha and V(p)) for TCC were obtained by thermodilution and hypertonic saline dilution, to yield absolute LV volume. Results indicate a good linear correlation with angiographic volume ( R(2)=0.78) with an intercept of 10+/-15 ml, not significantly different from 0 and slope of 1.17+/-0.16. Mean calibration factors alpha and V(p) were 0.017+/-0.002 (interpatient variability 0.018) and 75.1+/-0.4 ml (interpatient variability 35.4 ml), respectively. CONCLUSIONS: The TCC method provides on-line and continuous LV volume signals in patients in a relatively noninvasive way. Calibration yields absolute LV volumes with a good linear correlation in comparison to biplane LV angiography. TCC appears to be a promising methodology for monitoring absolute LV volume in the ICU.
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Hemodynamic characterization of left ventricular function in experimental coxsackieviral myocarditis: effects of carvedilol and metoprolol.
BACKGROUND: Carvedilol, a vasodilating nonselective beta-adrenoceptor antagonist, but not metoprolol, a selective beta1-adrenoceptor antagonist, has been shown to increase the production of cardiac antiinflammatory cytokines in experimental myocarditis. However, the hemodynamic consequences of these differences had not been investigated until today. Therefore, we determined the effects of carvedilol and metoprolol on left ventricular function in a murine model of coxsackievirus B3 (CVB3)-induced myocarditis. METHODS: BALB/c mice were inoculated with the coxsackie-B3 virus. Four and 10 days after infection, left ventricular function was investigated using a conductance micromanometer system. Additional groups were treated starting 24 h after infection using equipotent doses of carvedilol and metoprolol and studied on day 10. RESULTS: On day 4, infected mice manifested increased afterload-enhanced contractility and abnormal diastolic function. On day 10, contractile function of untreated mice was impaired. Carvedilol significantly improved cardiac index and most systolic indices, whereas metoprolol was substantially less effective. Diastolic dysfunction was not influenced by either of the beta-adrenoceptor antagonists. CONCLUSIONS: These hemodynamic data indicate that not only beta1-adrenoceptor blockade but also pleiotropic effects are involved in the cardioprotective effects of carvedilol on the pathophysiology of acute viral myocarditis.
Animals↗
Left ventricular pressure-volume measurements in mice: comparison of closed-chest versus open-chest approach.
OBJECTIVE: We investigated whether in vivo closed-chest left ventricular pressure-volume measurements would yield similar values for LV hemodynamics compared with open-chest PV measurements under several anesthetics. METHODS: The right common carotid of C57Bl/6 mice was cannulated with a combined pressure-conductance catheter and inserted retrogradely into the left ventricle in the closed-chest model. The open-chest model consisted of an abdominal approach involving the opening of the thoracic cavity by transverse opening of the diaphragm and ventricular catheterization by apical stab. Measurements were performed under urethane or pentobarbital intraperitoneal injection anesthesia. RESULTS: Cardiac function in the open-chest model was characterized by larger ejection fraction and stroke volume with a leftward shift in ventricular volume compared to the closed-chest model. Further observed characteristics include low end-systolic pressure and arterial-ventricular coupling mismatch in the open-chest model. Arrhythmias were not detected in either model. CONCLUSION: Murine cardiac function determination via open-chest or closed-chest protocols is sensitive, reproducible and comparable. The choice for open- or closed-chest pressure-volume measurements in mice depends on the aims of the study.
Animals↗
Comparison of benefits from cardiac resynchronization therapy in patients with ischemic cardiomyopathy versus idiopathic dilated cardiomyopathy.
Cardiac resynchronization therapy (CRT) is a recently introduced therapeutic option for patients with severe heart failure and intraventricular conduction disturbances. However, it is estimated that 20% to 30% of patients may not respond to CRT. Patients with ischemic cardiomyopathy (IC) may respond less favorably to CRT compared with patients with idiopathic dilated cardiomyopathy (IDC). Accordingly, the beneficial effects of CRT were evaluated in 2 subsets of patients (IC and IDC). Seventy-four patients with end-stage heart failure, New York Heart Association (NYHA) class III or IV, left ventricular (LV) ejection fraction <35%, QRS >120ms, and left bundle branch block received a biventricular pacemaker. At baseline and 6 months after implantation these parameters were evaluated: NYHA class, Minnesota quality-of-life score, QRS duration, and 6-minute walking distance. LV ejection fraction and severity of mitral regurgitation were assessed before and 6 months after CRT using 2-dimensional echocardiography. Long-term follow-up and hospitalization rates were obtained up to 2 years. Of the 74 patients, 46% (n = 34) had IC and 54% (n = 40) IDC. At 6 months follow-up all clinical parameters, QRS duration, LV ejection fraction, and mitral regurgitation improved significantly in both groups. Long-term (2-year) follow-up showed a survival rate of 87.5% for patients with IDC and 88.3% for patients with IC. The percentages of responders to CRT (defined as an improvement in NYHA class >or=1 grade) were comparable in both groups (65% vs 71%). Therefore, the underlying etiology of heart failure (IC vs IDC) was not related to the response to CRT.
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Dobutamine induces ineffective work in regional ischaemic myocardium: an experimental strain rate imaging study.
In the present study, we sought to investigate the effects of differing inotropic conditions on regional myocardial function in ischaemic segments. In an experimental pig model ( n =11), the regional deformation parameters peak systolic strain rate [SR(SYS) (peak velocity of thickening)], systolic strain [epsilon(SYS) (systolic wall thickening)] and post-systolic strain [epsilon(PST) (ongoing wall thickening after end of systole)] were measured during normal perfusion and regional ischaemia of the posterior wall. These parameters were compared with global contractility [E(ES) (end-systolic elastance)] measured by a conductance catheter. Ischaemia was induced by an active coronary hypoperfusion in the circumflex coronary artery. Measurements were done at baseline, during dobutamine and during esmolol infusion. In normal perfused hearts, SR(SYS) (4.8+/-0.2 s(-1) at baseline) increased during dobutamine infusion, decreased during esmolol infusion and correlated significantly with global E(ES). In addition, epsilon(SYS) averaged 93+/-3% at baseline and there was almost no epsilon(PST) (4+/-1%) in normal myocardium. In ischaemic myocardium, SR(SYS) and epsilon(SYS) were significantly reduced compared with normal myocardium at baseline (SR(SYS)=2.8+/-0.3 s(-1), and epsilon(SYS)=43+/-6%; P <0.001 compared with normal perfused hearts), whereas global E(ES) was unchanged. In contrast, epsilon(PST) was significantly increased in regional ischaemic segments compared with the non-ischaemic myocardium (15+/-2%; P <0.001). During the dobutamine infusion, SR(SYS) remained unchanged. In contrast, epsilon(SYS) decreased (25+/-5%; P <0.001) and epsilon(PST) increased (25+/-4%; P <0.05) significantly during dobutamine infusion in ischaemic myocardium. In ischaemic segments, an inotropic stimulation with dobutamine resulted in a shift of strain from systole (epsilon(SYS)) to post-systole (epsilon(PST)). Thus dobutamine induced ineffective myocardial work in ischaemic segments.
Adrenergic beta-Antagonists↗
Relationship between QRS duration and left ventricular dyssynchrony in patients with end-stage heart failure.
INTRODUCTION: Patients with end-stage heart failure and a wide QRS complex are considered candidates for cardiac resynchronization therapy (CRT). However, 20% to 30% of patients do not respond to CRT. Lack of left ventricular dyssynchrony may explain the nonresponse. Accordingly, we evaluated the presence of left ventricular dyssynchrony using tissue Doppler imaging (TDI) in 90 consecutive patients with heart failure. METHODS AND RESULTS: Ninety patients with severe heart failure (left ventricular ejection fraction <35%, New York Heart Association class III-IV) were prospectively evaluated. Based on QRS duration, 30 consecutive patients with a narrow QRS complex were included (QRS duration 150 ms). All patients underwent TDI to assess left ventricular dyssynchrony. Extensive left ventricular dyssynchrony was defined as an electromechanical delay on TDI between the septum and lateral wall, the so-called septal-to-lateral delay, of >60 ms. Severe dyssynchrony was observed in 27% of patients with narrow QRS complex, 60% with intermediate QRS duration, and 70% with wide QRS complex. No relation existed between QRS duration and septal-to-lateral delay. CONCLUSION: From 30% to 40% of heart failure patients with QRS duration >120 ms do not exhibit left ventricular dyssynchrony, which may explain the nonresponse to CRT. Alternatively, 27% of patients with heart failure and a narrow QRS complex show significant left ventricular dyssynchrony and may be candidates for CRT.
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